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成年大鼠暴露于>95％O_2中58h时,有半数以上动物死亡。外周血中白细胞计数先明显下降,后逐渐回升,至58h升至接近正常水平。支气管肺泡洗出液中,细胞总数和白细胞计数在10、17、34、58h均明显高于对照组。在34h至58h之间上升幅度加大(增加约一倍)。肺泡巨噬细胞数则明显低于对照组。支气管肺泡洗出液中蛋白含量和β-葡萄糖醛酸酶活性在死前(58h)升高非常明显,分别从34h的0.345±0.037至2.327±0.149mg/ml和4.67±1.02至17.34±1.85μg酚酞/ml/h。作者认为,高氧引起的肺的急性炎症性变化可能为动物致死的原为之一,高氧可能直接损伤肺泡巨噬细胞使之减少。
When adult rats were exposed to> 95% O2 for 58h, more than half of the animals died. Peripheral blood leukocyte count decreased significantly, then gradually rose to 58h rose to near normal levels. Bronchoalveolar lavage fluid, the total number of cells and white blood cell count at 10,17,34,58 h were significantly higher than the control group. Between 34h and 58h, the increase has increased (about doubled). Alveolar macrophages were significantly lower than the control group. The protein content and β-glucuronidase activity in bronchoalveolar lavage fluid were significantly increased before death (58h) from 0.345 ± 0.037 to 2.327 ± 0.149mg / ml and 4.67 ± 1.02 to 17.34 ± 1.85μg Phenolphthalein / ml / h. The authors suggest that the acute inflammatory changes in lungs caused by hyperoxia may be one of the original causes of lethality in animals, and hyperoxia may directly impair alveolar macrophages.